Summer Undergraduate Research Experience  >  Research Topics/Projects Available

Duchenne muscular dystrophy is an X-linked disorder caused by mutations in the gene dystrophin. The primary symptom of the disease is muscle degeneration, which becomes apparent in early childhood, and survival is rare beyond the early 30s. It is not entirely clear how mutations in the dystrophin gene lead to muscle degeneration, however, researchers have identified several molecules that are expressed abnormally throughout the course of the disease and are suspected to play a role in pathogenesis. One such molecule is the protein NF-kappaB. More NF-kappaB is activated, meaning that it is localized to the nucleus of the cell where it binds DNA, in muscle samples from mice and humans with Duchenne muscular dystrophy than in control samples. Additionally, drugs that decrease NF-kappaB activation in mice with Duchenne muscular dystrophy significantly reduce their muscle degeneration.

Working in collaboration with Dr. George Carlson at AT Still University, we would like to identify proteins which are potential members of the NF-kappaB pathway (can activate or be activated by NF-kappaB) and are expressed abnormally in mice with Duchenne muscular dystrophy. Not only will this give us a greater understanding of the molecular cascade of events that cause disease, but it will also provide more targets for drugs that may treat the disorder. We will search the literature to identify proteins which are potential members of the NF-kappaB pathway, and then we will investigate whether these proteins are expressed abnormally in mice with Duchenne muscular dystrophy by immunoblotting muscle extracts from affected mice and control mice using various antibodies.

Completion of Bio 107 (or equivalent) is strongly preferred. It will be helpful to have a basic understanding of the classes of biomolecules, cellular organization, transcription and translation.